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Despite the fact that it must infuriate Ian, Cambridge is also one of the leading research centers investigating the relationship between the loss of evolutionary normal conditions and the subsequent rise in incidence of inflammatory diseases.
Bob

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My younger son has ulcerative colitis and was recently hospitalized for a week. His specialist is a physician from India. The doctor told him that UC is a Caucasian disease and that it is rarely seen in India, Asia or Africa.

He also told him basically what is presented in the article you posted.

gwa wrote:He also told him basically what is presented in the article you posted.

You made my day gwa and I needed that!

I recently contacted one of the writers of that article, Professor Anne Cooke, and this is an excerpt:

> Most autoimmune researchers seem to be convinced that incidence of > autoimmune disease is owed to genetic predisposition and then an > environmental trigger(s) to set the autoimmunity ball in motion. I would say that it is more balanced now with increasing numbers considering the alternative view that infection might have hitherto inhibited the development of some autoimmune conditions.>> The basis of research is comparison and all autoimmune disease > research to my awareness has compared people with autoimmune disease > in developed populations to people without autoimmune disease in > developed populations. It seems that comparison might be akin to > comparing someone with disease to someone with predisposition. > Obviously not the most favorable research situation. Kind of like > comparing an orange to an orange. You're not going to discover many > differences by looking at basically the same thing.> > My question is....do you know of any autoimmunity research actually > focusing on a comparison between the systems of those in undeveloped > countries with situations which are seen in autoimmunity?There is a research interest in doing just that. Some Scandinavian researchers were proposing to look at two populations which are genetically rather similar but living in different conditions- Scandinavia versus Eastern European countries.

gwa wrote:The doctor told him that UC is a Caucasian disease

This is NOT meant to be negative but I think evidence is starting show that it's time to eliminate that MS "truism".

Although (using blacks as an example) blacks in Africa ("undeveloped") rarely experience inflammatory disease and although incidence data does reflect that blacks in the US ("developed") experience lower MS rates than whites, it's important to consider that the "hygiene hypothesis" more accurately reflects financial status and living conditions than "hygiene" Per se.

It also seems necessary to dispose of the genetic MS "truisms" based on genetics in which lighter skinned people are more genetically inclined to MS and that darker skinned people closer to the equator are less genetically inclined to MS, when considering the locations and complexion color of the populations which "developed" first and in reality remain among the areas of the world which are "developed" ("developed"=common availability of electricity, running water and flush toilets).

It's not hard to determine that the populations of the developed countries are and have always been primarily white and that those locations in which they populate, are and have always been more distant from the equator.

Is MS geographic prevalence really attributable to the long held assumptions regarding genetics or did the researchers long ago overlook the fact that the MS geographic incidence data also depicts a world map of economic wealth/development?

Regarding the current lower MS rates among blacks (or any darker complexion in the US) who has always been on the bottom of the economic totem pole and has experienced the poorer living conditions? Obviously those of darker persuasion.

The incidence figures we are familiar with have always been general, non specific averages. I THINK if someone were to do an MS incidence study and included Montel, Richard Pryor and all the other wealthy black Americans, they would show exactly the same incidence rate as U.S. Caucasians.

I've been corresponding with Dr Kurtzke about the loss of evolutionary normal conditions as a precursor to immune dysfunction in the attempt to convince him to investigate and form his own opinion. I'm convinced a little effort and an open mind would lead any intelligent person to become convinced.

I won't lie, the involvement of a name like Dr Kurtzke's would accelerate serious consideration in the science community, but what caused me to initially contact him was my recently reading his 1993 paper "Epidemiologic Evidence for Multiple Sclerosis as an Infection" in which he had done an awesome job of weighing every possible considerable factor at that point in time and came to the conclusion that the British troops must have spread MS in the Faroes by an, as yet, unidentifiable infection.

What his arrived conclusion meant to me is that one of the last researchers to realize that we can't cure MS until we can label the cause and one of the best minds in MS research went over all the information in this very contained and specific situation (Faroe "outbreak") and came to the conclusion that everything pointed towards the British soldiers spreading some undefinable infection among the residents of the Faroes, which even in 1993 (and 2007) was beyond our ability to confirm or identify.

I simply wanted to point out to Dr Kurtzke that if the British presence "eliminated" something which had always been present in the Faroe population, it would present the EXACT same picture as the introduction of his "unidentifiable infection".

Might the thing which the British presence (and influence) eliminated from the periphial Faroe residents have been their historic parasite infestations?

Bob

(Final comments from "Epidemiologic Evidence for Multiple Sclerosis as an Infection")

COMMENTSThe best measures of the geographic distribution of MScome from prevalence studies, of which there are now over300. These works indicate that, geographically, MS is distributedthroughout the world within three zones, of high,medium, and low frequency. High-frequency areas, withprevalence rates of 30 or more per 100,000 population, nowmostly 50 to 120 per 100,000, comprise northern and centralEurope into Italy and the former USSR, Canada, the northernUnited States, New Zealand, and southeastern Australia.These regions are bounded by areas of medium frequency,with prevalence rates of 5 to 29 per 100,000population and comprising much of Australia; the southernUnited States; southwestern Norway; northernmost Scandinavia;much of the northern Mediterranean basin and possiblyits eastern and southern shores as well; probably Russiafrom the Urals into Siberia as well as the Ukraine; SouthAfrica (whites); and perhaps central South America. Allother studied areas of Asia, Africa, and the Caribbeanregion, including Mexico and possibly northern South America,are all of low frequency, with prevalence rates of lessthan 5 per 100,000 population. A number of nationwideprevalence studies in Europe provide evidence for geographicclustering of the disease, which is stable over time,but with, however, evidence of diffusion over time as well.There is a female preponderance in incidence, prevalence,and mortality rates of about 1.5:1 (female/male). Annualincidence rates are about 3 to 5 per 100,000 population inhigh-risk areas, about 1 per 100,000 in medium-risk areas,and about 1 per 1,000,000 in low-risk areas. Age-specificincidence rates rise from 0 in childhood through adolescenceto a peak close to age 27 and then return more slowly to 0 byage 60. This pattern is what one might expect for aninfectious disease with a limited age range of susceptibility.All high- and medium-risk areas are among predominantlywhite populations: MS is a white female burden. In theUnited States, blacks, Orientals, and possibly AmericanIndians have much lower rates of MS than do whites, but each group still demonstrates the geographic gradients foundfor whites.Aside from geography, age, sex, and race, risk factors forMS include high socioeconomic status and level of urbanizationof preillness residence, at least in the U.S. Armyseries. No meteorologic correlate of geography is a riskfactor for MS when latitude is controlled. In the UnitedStates, there is a strong correlation of MS risk with populationswith Scandinavian, particularly Swedish, ancestry.There is an increased familial frequency in MS. Twinstudies are inconclusive in terms of a genetic component,and I believe that the familial excess reflects commonenvironment more than common genes.Migration studies indicate that, on the whole, migrants donot retain all of the risk of their birthplace. MS risk is clearlynot defined at birth: MS death rates for migrants born in onerisk area and dying in another are intermediate betweenthose characteristic of their birthplace and their death residence,regardless of the direction of the move. Prevalencestudies for migrants from high- to low-risk areas indicate ageof adolescence to be critical for risk retention; those migratingabove age 15 retain the MS risk of their birthplace, andthose migrating below age 15 acquire the lower risk of theirnew residence. Thus, in high-risk areas of endemicity, MS isacquired in early adolescence, and young children are notsusceptible to the disease. Several studies of migrants movingfrom low- to high-risk areas show that those migrating inchildhood or older do in fact increase their risk of MS, withage 10 or 11 apparently being the minimum age of susceptibilityand about ages 40 to 45 being the maximum. Themigrant data and the geographic distributions serve to defineMS as an acquired, exogenous, environmental disease with aprolonged incubation period between acquisition and clinicalexpression-a situation most compatible with an infectiousdisease with prolonged latency.MS on the Faroe Islands has occurred as four successiveepidemics beginning in 1943. The disease was introduced byBritish troops who occupied the islands for 5 years from1940. What they introduced must have been an infection,which is called PMSA.In this concept, PMSA is a single widespread systemicinfectious disease (perhaps asymptomatic) that only rarelyleads to CNMS after an incubation period averaging 6 yearsfor virgin populations (and 12 years for populations in areasof endemicity). It requires 2 (for the former populations) orpossibly 4 (for the latter populations) years of exposurebefore the disease is acquired. Susceptibility to PMSA islimited to about ages 11 to 45 at the start of exposure;transmissibility ends at about age 26.If the PMSA agent has these characteristics of prolongedexposure, limited age of susceptibility, prolonged incubation,and rare clinical disease, then the geographic spread ofthis disorder would also be prolonged. In this manner, onecould explain the current distribution of MS as the result ofslow diffusion from an origin in the lower Scandinavianpeninsula at or before the start of the 18th century, withoverseas spread by migrations: Scandinavians to America inthe mid-19th century and British to Australia, New Zealand,and South Africa rather later.Thus, I believe that clinical MS is the rare late outcome ofa specific but unknown infectious disease of adolescence andyoung adulthood and that this infection could well be causedby a thus-far-unidentified (retro)virus.

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